J Cancer 2017; 8(12):2277-2281. doi:10.7150/jca.19677 This issue Cite
Research Paper
1. State Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China;
2. Department of Thoracic Surgery, Shanghai Pulmonary Hospital (Tongji University), Shanghai 200433, China;
3. Department of General Surgery, the branch of Shanghai First People's Hospital, Shanghai 200081, China
4. Department of Pharmacy, Xin-hua Hospital Affiliated to Medical School, Shanghai Jiao Tong University, Shanghai 200092, China
5. Department of Pharmacy, the branch of Shanghai First People's Hospital, Shanghai 200081, China
Histone acetyltransferases (HATs) play vital functions in the tumorigenesis of many solid organ malignancies. We previously screened a human HATs cDNA library and identified Tat-interactive protein-60KDa (TIP60) as a candidate critical HATs in the origination of lung cancer. In this study, our data suggested that overexpression of TIP60 inhibited the cell viability of A549 and H1299 cells since day 2. Compared to the control group, the viability of these two lung cancer cells was inhibited by 25% and 19% at day 6 with the overexpression of TIP60. It increased by 36% and 26% when TIP60 was knockdown for 6 days. The invasion ability of these two cells was also restrained when TIP60 was overexpressed. While knockdown of TIP60 had the opposite effect. Inhibition of TIP60 significantly promoted the expression of molecules in AKT signaling pathway especially c-Myc. Furthermore, compared to paired tumor-adjacent tissue, lung cancer tumors had low expression of TIP60. Therefore, we concluded that TIP60 might inhibit the viability and invasion ability of lung cancer cells through down-regulation of AKT signaling pathway.
Keywords: TIP60, lung cancer, cell viability, AKT, Myc